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弱视的神经基础:综述

Neuronal basis of amblyopia: a review.

作者信息

Grigg J, Thomas R, Billson F

机构信息

Department of Clinical Ophthalmology, University of Sydney, NSW, Australia.

出版信息

Indian J Ophthalmol. 1996 Jun;44(2):69-76.

PMID:8916592
Abstract

Amblyopia is an acquired defect in vision due to an abnormal visual experience during a sensitive period of visual development. The neuronal basis of amblyopia is the study of the effects of "abnormal" environmental influences on the genetically programmed development of the visual processing system. Visual pathway development commences with ganglion cells forming the optic nerve. The process that guides these neurones initially to the lateral geniculate nucleus (LGN) and then onto the visual cortex is genetically programmed. Initially this process is influenced by spontaneously generated impulses and neurotrophic factors. Following birth, visual stimuli modify and refine the genetically programmed process. Exposure to the visual environment includes the risk of abnormal inputs. Abnormal stimuli disrupt the formation of patterned inputs allowing alteration of visual cortical writing with reduction in ocular dominance columns driven by the abnormal eye. Correction of the abnormal visual input and penalisation of the "normal" input is the mainstay of therapy for amblyopia. Further understanding of the mechanisms involved in the development of a normal visual processing system will allow trialing therapies for amblyopia not responding to occlusion therapy. Levodopa is one agent providing insights into recovery of visual function for short periods in apparently mature visual systems.

摘要

弱视是一种由于视觉发育敏感期的异常视觉经历而导致的后天性视力缺陷。弱视的神经学基础是研究“异常”环境影响对视觉处理系统基因编程发育的作用。视觉通路的发育始于形成视神经的神经节细胞。引导这些神经元最初到达外侧膝状体核(LGN),然后到达视觉皮层的过程是由基因编程的。最初,这个过程受自发产生的冲动和神经营养因子的影响。出生后,视觉刺激会改变和完善基因编程的过程。暴露于视觉环境中存在异常输入的风险。异常刺激会破坏模式化输入的形成,从而改变视觉皮层的布线,减少由异常眼驱动的眼优势柱。纠正异常视觉输入并抑制“正常”输入是弱视治疗的主要方法。进一步了解正常视觉处理系统发育所涉及的机制,将有助于试验对遮盖疗法无反应的弱视治疗方法。左旋多巴是一种能让我们了解在明显成熟的视觉系统中短期内视觉功能恢复情况的药物。

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